To the Editor.—Extensive postmortem studies on 4 patients autopsied after infection with West Nile virus (WNV) in Mississippi demonstrated injury to spinal and sympathetic ganglia mirrored by damage to the spinal gray matter. The disappearance of sympathetic neurons was incriminated for the autonomic instability observed in some WNV patients.1 That could well be responsible for any observed labile vital signs, hypotension, and potentially lethal cardiac arrhythmias. Fundamental information about the neurological changes linked with WNV could as well be determined with imaging techniques like magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS).
Imaging techniques have addressed some of the fundamental features of viral replication in the central nervous system. For example, MRI of the cervical spine of a 27-year-old man who developed acute flaccid paralysis 3 weeks after his 20-month-old infant was immunized with live poliovirus vaccine revealed smooth hyperintense bands. Sagittal proton-density T2-weighted images revealed involvement of the regions corresponding to the anatomic locations of ventral horns.2
Examination of a 13-year-old girl with subacute sclerosing panencephalitis during MRS to establish any in vivo pathophysiologic abnormalities was intriguing. Both inflammatory processes and glial proliferation were evident prior to neuronal loss visible in MRI-negative as well as MRI-positive regions.3 Furthermore, 3 patients with Creutzfeldt-Jakob disease showed evidence of reduced N-acetylaspartate–creatine ratios on MRS. These changes implied that neuronal loss and/or dysfunction were a consistent feature of established Creutzfeldt-Jakob.4
Using imaging techniques on survivors of WNV infection and future patients with a neurological manifestation would be intriguing. West Nile virus encephalitis was also responsible for fatal encephalitis during its transmission from an organ donor to a kidney transplant recipient. There were extensive postmortem viral encephalopathic changes. Immunohistochemical studies had highlighted WNV antigens within neurons, especially in the cerebellum and brainstem.5